scholarly journals Quality-Control Mechanism for Telomerase RNA Folding in the Cell

Cell Reports ◽  
2020 ◽  
Vol 33 (13) ◽  
pp. 108568
Author(s):  
Xichan Hu ◽  
Jin-Kwang Kim ◽  
Clinton Yu ◽  
Hyun-Ik Jun ◽  
Jinqiang Liu ◽  
...  
Keyword(s):  
Quality Control ◽  
Rna Folding ◽  
Control Mechanism ◽  
Telomerase Rna ◽  
Quality Control Mechanism

Overexpression of Buffy enhances the loss of parkin and suppresses the loss of Pink1 phenotypes in Drosophila

Genome ◽  
2017 ◽  
Vol 60 (3) ◽  
pp. 241-247
Author(s):  
P. Githure M’Angale ◽  
Brian E. Staveley
Keyword(s):  
Gene Expression ◽  
Quality Control ◽  
Early Onset ◽  
Autosomal Recessive ◽  
Control Mechanism ◽  
Nigrostriatal Neurons ◽  
Climbing Ability ◽  
Quality Control Mechanism ◽  
Locomotor Ability ◽  
Early Onset Parkinson’S Disease

Mutations in parkin (PARK2) and Pink1 (PARK6) are responsible for autosomal recessive forms of early onset Parkinson’s disease (PD). Attributed to the failure of neurons to clear dysfunctional mitochondria, loss of gene expression leads to loss of nigrostriatal neurons. The Pink1/parkin pathway plays a role in the quality control mechanism aimed at eliminating defective mitochondria, and the failure of this mechanism results in a reduced lifespan and impaired locomotor ability, among other phenotypes. Inhibition of parkin or Pink1 through the induction of stable RNAi transgene in the Ddc-Gal4-expressing neurons results in such phenotypes to model PD. To further evaluate the effects of the overexpression of the Bcl-2 homologue Buffy, we analysed lifespan and climbing ability in both parkin-RNAi- and Pink1-RNAi-expressing flies. In addition, the effect of Buffy overexpression upon parkin-induced developmental eye defects was examined through GMR-Gal4-dependent expression. Curiously, Buffy overexpression produced very different effects: the parkin-induced phenotypes were enhanced, whereas the Pink1-enhanced phenotypes were suppressed. Interestingly, the overexpression of Buffy along with the inhibition of parkin in the neuron-rich eye results in the suppression of the developmental eye defects.

Where Parkin Parks

2013 ◽  
Vol 6 (273) ◽  
pp. ec96-ec96
Author(s):  
L. Bryan Ray
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Quality Control ◽  
Protein Kinase ◽  
Full Text ◽  
Control Mechanism ◽  
Membrane Depolarization ◽  
Mitofusin 2 ◽  
Link Type ◽  
Quality Control Mechanism

Damaged mitochondria are removed from cells in a process known as mitophagy. Failure of this quality-control mechanism contributes to Parkinson’s disease. When damaged mitochondria lose membrane depolarization, the protein kinase, PINK1, accumulates on the mitochondrial surface, recruits Parkin, and promotes mitophagy. Chen and Dorn describe another component of this process, mitofusin 2, which appears to function as the receptor for Parkin on the surface of damaged mitochondria.Y. Chen, G. W. Dorn II, PINK1-phosphorylated mitofusin 2 is a Parkin receptor for culling damaged mitochondria. Science340, 471–475 (2013). [Abstract] [Full Text]

scholarly journals Peters Plus Syndrome Mutations Disrupt a Noncanonical ER Quality-Control Mechanism

2015 ◽  
Vol 25 (3) ◽  
pp. 286-295 ◽  
Author(s):  
Deepika Vasudevan ◽  
Hideyuki Takeuchi ◽  
Sumreet Singh Johar ◽  
Elaine Majerus ◽  
Robert S. Haltiwanger
Keyword(s):  
Quality Control ◽  
Control Mechanism ◽  
Er Quality Control ◽  
Quality Control Mechanism
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